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首页> 外文期刊>Cellular Physiology and Biochemistry >Acute Respiratory Distress Syndrome Induced by White Smoke Inhalation: a Potential Animal Model For Evaluating Pathological Changes and Underlying Mechanisms
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Acute Respiratory Distress Syndrome Induced by White Smoke Inhalation: a Potential Animal Model For Evaluating Pathological Changes and Underlying Mechanisms

机译:吸入白烟引起的急性呼吸窘迫综合征:评估病理变化和潜在机制的潜在动物模型

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Background/Aims White smoke inhalation (WSI) is an uncommon but potentially deadly cause of acute respiratory distress syndrome (ARDS). However, no clinical treatment protocol has been established for the treatment of WSI-induced ARDS. Therefore, it is necessary to investigate the effects of WSI in ARDS and the mechanisms underlying the effects of WSI to determine a novel therapeutic target. Methods On the basis of the duration of continued inhalation of white smoke (3 min, 5 min, and 7 min), rats were divided into three groups (WSI-3 min, WSI-5 min, and WSI-7 min). The survival rate, pathological change, and computed tomography (CT) score were evaluated to determine the modeling conditions. In the established WSI-5 min models, evaluations were performed to evaluate the following arterial blood gas levels, lung wet/dry weight ratio, the expression of inflammatory cytokines, and the effect of NF-κB signaling pathway. Results The survival rate of rats at 72 h post-WSI in the WSI-3 min, WSI-5 min, and WSI-7 min groups was 83.33%, 75%, and 25%, respectively. Results from evaluation of H&E staining, CT scan, arterial blood gas levels, and lung wet/dry weight ratio suggest that the pathological changes in the rat in the WSI-5 min and WSI-7 min groups are very similar to those in patients with ARDS induced by WSI. Additionally, the expression of INF-γ, TGF-β1, TNF-α, and IL-1β were increased, and the NF-κB signaling pathway was activated in the WSI-5 min group. Conclusion The rat model of WSI-5 min can be used as a WSI-induced ALI model for further experiments. The NF-κB signaling pathway may be a potential therapeutic target for the treatment of WSI- induced ARDS.
机译:背景/目的吸入白烟(WSI)是一种罕见的但可能致命的急性呼吸窘迫综合征(ARDS)病因。但是,尚未建立用于治疗WSI诱导的ARDS的临床治疗方案。因此,有必要研究WSI在ARDS中的作用以及WSI影响基础的机制,以确定新的治疗靶标。方法根据持续吸入白烟的时间(3分钟,5分钟和7分钟),将大鼠分为三组(WSI-3分钟,WSI-5分钟和WSI-7分钟)。评估存活率,病理变化和计算机断层扫描(CT)评分以确定建模条件。在已建立的WSI-5分钟模型中,进行评估以评估以下动脉血气水平,肺干/湿重比,炎性细胞因子的表达以及NF-κB信号通路的作用。结果在WSI-3分钟,WSI-5分钟和WSI-7分钟组中,WSI后72小时大鼠的存活率分别为83.33%,75%和25%。 H&E染色,CT扫描,动脉血气水平和肺干湿比的评估结果表明,WSI-5分钟和WSI-7分钟组大鼠的病理变化与WSI诱发的ARDS患者中的那些。此外,WSI-5 min组中INF-γ,TGF-β1,TNF-α和IL-1β的表达增加,并且NF-κB信号通路被激活。结论WSI-5 min大鼠模型可作为WSI诱导的ALI模型用于进一步的实验。 NF-κB信号通路可能是治疗WSI诱导的ARDS的潜在治疗靶标。

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